Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection versus Immunopathology.
Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection versus Immunopathology.
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DOI：
10.1186/1710-1492-4-1-2
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发表时间：
2008-03-15
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影响因子：
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通讯作者：
Dhabhar FS
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作者：
Dhabhar FS
人们普遍认为，压力会抑制免疫功能，增加感染和癌症的易感性。矛盾的是，压力还会加重过敏性、自身免疫性和炎症性疾病。这些观察表明，压力可能对免疫功能有双向影响，在某些情况下是免疫抑制，在另一些情况下是免疫增强。最近的研究表明，与抑制或失调免疫功能的慢性应激不同，急性应激可以增强免疫功能。急性应激可促进树突状细胞、中性粒细胞、巨噬细胞和淋巴细胞的运输、成熟和功能，并已被证明能增强先天和获得性免疫反应。在新抗原暴露前经历的急性应激可增强先天免疫和记忆性T细胞的形成，并导致显着和持久的免疫增强。在抗原再暴露过程中经历的急性应激可增强二次/适应性免疫反应。因此，根据免疫激活的条件和免疫抗原的不同，急性应激可能会增强免疫保护或免疫病理的获得和表达。相比之下，慢性应激通过改变1型和2型细胞因子平衡来调节先天和获得性免疫反应，并通过减少白细胞数量、运输和功能来抑制免疫。慢性应激还通过抑制1型细胞因子和保护性T细胞，同时增加抑制性T细胞功能，增加患皮肤癌的易感性。我们认为，生理应激反应的适应目的可能是促进生存，应激激素和神经递质充当灯塔，为免疫系统准备应对大脑感知的潜在挑战(例如，伤害或感染)(例如，检测攻击者)。然而，如果增强的免疫反应是针对无害或自身抗原的，或者在长期激活后调节失调，就像在慢性应激期间一样，这种系统可能会加剧免疫病理。鉴于应激的普遍性质及其对免疫保护和免疫病理的显著影响，进一步阐明调节应激-免疫相互作用的机制并将研究结果从实验台到床边进行有意义的转换是很重要的。
It is widely believed that stress suppresses immune function and increases susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate allergic, autoimmune, and inflammatory diseases. These observations suggest that stress may have bidirectional effects on immune function, being immunosuppressive in some instances and immunoenhancing in others. It has recently been shown that in contrast to chronic stress that suppresses or dysregulates immune function, acute stress can be immunoenhancing. Acute stress enhances dendritic cell, neutrophil, macrophage, and lymphocyte trafficking, maturation, and function and has been shown to augment innate and adaptive immune responses. Acute stress experienced prior to novel antigen exposure enhances innate immunity and memory T-cell formation and results in a significant and long-lasting immunoenhancement. Acute stress experienced during antigen reexposure enhances secondary/adaptive immune responses. Therefore, depending on the conditions of immune activation and the immunizing antigen, acute stress may enhance the acquisition and expression of immunoprotection or immunopathology. In contrast, chronic stress dysregulates innate and adaptive immune responses by changing the type 1-type 2 cytokine balance and suppresses immunity by decreasing leukocyte numbers, trafficking, and function. Chronic stress also increases susceptibility to skin cancer by suppressing type 1 cytokines and protective T cells while increasing suppressor T-cell function. We have suggested that the adaptive purpose of a physiologic stress response may be to promote survival, with stress hormones and neurotransmitters serving as beacons that prepare the immune system for potential challenges (eg, wounding or infection) perceived by the brain (eg, detection of an attacker). However, this system may exacerbate immunopathology if the enhanced immune response is directed against innocuous or self-antigens or dysregulated following prolonged activation, as seen during chronic stress. In view of the ubiquitous nature of stress and its significant effects on immunoprotection and immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.